Hepatic stellate cells in alcoholic liver cirrhosis: mechanisms of fibrogenesis, plasticity, and fibrosis reversal.

Abstract

Objectives: To critically synthesize current mechanistic and clinical evidence on the role of hepatic stellate cells (HSCs) in alcoholic liver cirrhosis, with emphasis on fibrogenesis, cellular plasticity, fibrosis regression, and emerging diagnostic implications.

Evidence acquisition: A narrative review of literature was conducted using PubMed, Scopus, and Web of Science to identify relevant studies on hepatic stellate cells and their role in liver cirrhosis, with emphasis on recent mechanistic and translational research.

Results: HSCs are central mediators of fibrogenesis in alcoholic liver disease, contributing to extracellular matrix remodeling, immune signaling, and vascular alterations. Emerging evidence highlights the dynamic and potentially reversible nature of HSC activation, with distinct roles for apoptosis, senescence, and inactivation pathways. Recent studies also emphasize the influence of metabolic stress, gut-liver axis interactions, and micronutrient imbalances on HSC behavior. These insights support the development of targeted antifibrotic strategies and biomarker-driven approaches for disease monitoring.

Conclusion: HSCs are central drivers of fibrogenesis, vascular remodeling, and immune metabolic crosstalk in alcoholic liver cirrhosis. Integrating HSC-focused molecular profiling with non-invasive diagnostics and robust clinical endpoints is essential for the development of effective antifibrotic strategies.